Good Article Review On A Brief Overview Of HIV Virology And Pathogenetic Mechanisms

Published: 2021-06-18 05:20:08
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Category: Aliens, Viruses, Disease, Al, Genetics, Protein, Aids, DNA

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Human Immunodeficiency Virus, a main cause of worldwide AIDs, belongs to the Lentivirus genus of Retroviridae family. Pathogen causes chronic type of symptoms, taking a long time of latency it constantly keeps replicating inside human body. HIV is categorised into two types, HIV-1 and HIV-2. The genome of this retrovirus consists of two single-stranded RNA molecules. Though, both are involved in AIDS, HIV-2 seemed less virulent and demonstrated more frequent connections with the disease of central nervous system (Fanales-Belasio et al. 5).
Like other retroviruses, the genes located on HIV chromosome are gag, pol, env. The functions of gag, pol and env gene are encoding of structural proteins, encoding of viral envelope glycoproteins, and encoding of viral replication enzymes, respectively. The enzymes encoded by env gene are reverse transcriptase that transforms viral RNA into DNA, protease that slice large protein precursors of Gag and Pol, and integrase that integrates viral DNA into the DNA of host chromosome. The other regulatory genes of HIV that are involved in different significant processes and encode proteins include the tat, rev and vif protein. Tat encodes for Tat protein responsible for the expression of HIV genes. The Rev protein of rev genes verifies the transportation of genomic RNA and mRNA from nucleus to the cytoplasm. Vif gene encodes a small Vif protein that improves the pathogenicity of virus progeny particles. The several other proteins are Vpr, Vpu and Nef. Vpr helps reverse transcribed DNA to enter non-dividing nucleal cells such as macrophages. In HIV-2, this function is taken over by Vpx protein. Vpu facilitates the release of the virus particle, and Nef protein illustrates multiple functionalities including regulation of the CD4 receptor to assist virus budding and cellular signal transduction during replication cycle (Fanales-Belasio et al. 7).
The HIV replication involves six major steps: binding and entrance to the target cell, uncoating of capsid, reverse transcription and provirus integration, virus protein synthesis and assembly and budding. The initial step of viral binding involves envelope trimeric complex, and CD4 protein that gives a strong attachment of the virus. Binding is followed by fusion through penetration of the cell membrane permitting viral capsid to enter the cell. Now virus core opens up into the cytoplasm of target cell releasing the viral RNA, and it transforms into proviral DNA through the enzyme integrase and reverse transcriptase. The integration process and expression of progeny need the target cell in the active state. Therefore, macrophages, latently infected CD4+ T-cells are significant cellular reservoirs of HIV. On cell activation, transcribed DNA turns into a messenger RNA and early synthesis of regulatory proteins. Viral mRNA codes for long fragments moves towards cytoplasm, and structural components of new virions are shaped (Fanales-Belasio et al. 8).
Now replication enzymes help two strands of viral RNA to join and the core protein accumulate over them to form virus capsid. This new and immature particle drifts to the cell surface. HIV-1 protease slices the large precursor molecules forming new infectious viral particles. Variability of HIV permits virus to conquer host immunity as well as the impacts of therapeutic vaccines and drugs (Fanales-Belasio et al. 9).
The development of disease and the pathogenicity of HIV depends on the biologic properties of infecting virus isolate and the immune resistant capability of host. HIV cannot stay alive in the external environment and easily inactivated on the exposure with common disinfectants. The HIV transmission occurs through infected blood or bodily secretions via sharp tools or abrasions in mucosal tissues of genitals. Heterosexual intercourse is the most common cause of worldwide HIV infection. Viral RNA is detectable after 10-12 days post-infection, in the blood sample using RT-PCR amplification methods (Fanales-Belasio et al. 10).
Thus, the window period when infection exists but antibodies are not evident, often takes more than three months suggesting that the HIV-specific antibodies development requires a long period. Most of the infected individuals develop flu-like or mononucleosis-like symptoms from few days to several weeks. The inception of acute infection results in a clinically asymptomatic period with a drop in HIV viremia levels. In this period the HIV- pathogenic effects of HIV persevere and stimulate a slow and progressive loss of CD4+ lymphocytes that results in the damage to the immune system (Fanales-Belasio et al. 11).
Work Cited
Fanales-Belasio, Emanuele, et al. "HIV virology and pathogenetic mechanisms of infection: a
brief overview." Annali dell'Istituto superiore di sanita 46.1 (2010): 5-14.

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